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PERIODONTAL MICROBIOLOGY:

Bacterial plaque is the primary cause of gingivitis and the various forms of periodontitis.Although oral microbiota comprise of over 300species, only about 30 of these are considered to be

periodontopathic.

Periodontal health results from a host-parasite equilibrium that is characterized by minimal tissue

destruction and maximum repair of damaged structures.Alteration of this equilibrium may result as a result of local or systemic changes that decreases hostresistance or from quantitative and/or qualitative alteration of the periodontal microbiota, especially a

increase in virulence.

CRITERIA FOR PERIODONTOPATHOGENECITY OF A MICROORGANISM:

Socranskys theories of possible modes of progression of chronic destructive periodontal disease:

a- Progressive loss of attachment some sites show progressive loss of attachment over time

whereas other sites show no destruction. The time of onset and extent of destruction vary from

site to site.

b- Random burst model activity occurs at random at any site. Some sites show no activity,whereas other sites show one or several bursts of activity. The cumulative effect of destruction

may vary from site to site.

c- Asynchronous multiple burst model several sites show bursts of activity over a finite period

followed by prolonged periods of inactivity. Majority of disease activity takes place within a

few years.

Kochs postulates (1870) = classic basis to establish a specific micro-organism may be defined as the

causative agent for a human diseasei- always associatedwith the disease

ii- be routinely isolatedfrom the diseased individual

iii- be able to be grown in vitro cultures

iv- produce a similar disease when inoculated in animal studies

v- be recovered from lesions in diseased lab animals

vi- show specific immunologic changes in the human

Nature of periodontal diseases present difficulties in studying the periodontal microbiota and an

inability to apply the Kochs postulates.

i. The chronic nature of periodontal disease shows an episodic nature with alternating periods ofexacerbation and remission. Therefore any microbial analysis must take into account the stage of

disease activity at that location.

ii. The host resistance may be variable and difficult to measure.

iii. Results noted in animal models may not be directly transferable to a human model

iv. To access the changes of microbiota to treatment, it is difficult to define the criteria for success

v. Difficulties in sampling, dispersion and cultivation of the resident micro-organisms, becausebacteria from a diseased site may be pooled with that of healthy site. Samples usually contained

more material from supra-gingival plaque.


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vi. Lack of a well developed technique for maintaining a continuous anaerobic environment during

sampling harvesting and culture.

vii. Inadequate and ever evolving taxonomy.

Socransky suggested an alternative to Kochs postulates to label periodontal micro-organisms as

possible periodontopathogens.

1. the number of etiologic organisms in the pathologic sites must be increased and conversely the

number of organisms must be reduced or absent in healthy site or sites with other forms of disease2. if the etiologic organism is eliminated or suppressed, the disease should stop. If it doesnt stopeither the wrong organism was eliminated or organisms that remain in the site are sufficient by

themselves to enable destruction to continue.

3. an increase or decrease in cellular and/or humoral immune response to a given species in a

specific form of periodontal disease suggests a role for that organism in the disease process.

4. the micro-organism should be attempted to be isolated in pure culture and replication of anim

pathogenicity should be shown5. bacterial virulence factors responsible for enabling the micro-organism to cause destruction o

the periodontal tissues must be demonstrated.

DENTAL PLAQUE:

Definition: Dental Plaque is a specific host associated biofilm on tooth surface, restorations,orthodontic appliances and prosthesis that consists primarily of proliferating micro-organisms,

along with a scattering of epithelial cells, leukocytes, and macrophages in an adherent intercellular

matrix.

It is different from other tooth associated aggregations like pellicle, food debris, material alba and

calculus based upon its specificity, location, bacterial content and matrix.

Materia alba is the tooth associated biofilm consisting of bacterial aggregations, leukocytes anddesquamated oral epithelial cells accumulating at the surface of the teeth, but lacking the internal

structure observed in dental plaque.

Dental plaque lacks mineralization like calculus.

Classification: based upon its relation to gingival margin

- supragingival plaque

coronal plaque that plaque in contact with only the tooth surface

marginal plaque associated with tooth surface at the gingival margin

- sub gingival plaque

Supragingival Plaque

Visibility: It can be detected clinically only when it reaches a certain thickness. Small amounts are not

visible and can only be detected by using plaque disclosing agents.

Colour: When it accumulates becomes a visible globular mass with a nodular surface having a gray

to yellowish gray to yellow colour.Site: regularly at gingival third, especially surface cracks, pits, fissures of occlusal surfaces,

overhanging margins.


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That is sites protected from the normal mechanical cleansing action of the tongue, the cheeks, and

the lips.

Other sites include restorations, artificial crowns, orthodontic bands, dental implants, orthodonticappliances and prosthesis.

Quantity: measurable amounts within 1hour after the teeth are thoroughly cleaned and maximum in

about 30days or less.

Rate of formation: varies among individuals, on different teeth in same mouth, and different areas of

same toothInfluenced by - diet

- age

- salivary factors

- oral hygiene

- tooth alignment

- systemic disease

- host factors- mechanical retention factors

Composition: 70-80% = 200-400 different species bacteria in a complex arrangement

1 cubic mm of dental plaque with weight 1mg has about 108 bacteria

Other micro-organisms are mycoplasma, yeasts, protozoa, virus in different proportions

Non bacterial portion is interbacterial matrix = 20-30% plaque volume.Organic portion polysaccharide protein complex

Extra cellular products of plaque bacteria,

Cytoplasmic and cell membrane remnants

Food debris

Derivatives of salivary glycoproteins

30% carbohydrate9.5% of total plaque = dextran (bacteria produced polysaccharide)

Levan, galactose, rhamnose, and sometimes mutan30% protein

15% lipid

Remainder = note determined

Inorganic component very small quantity, and nil in early plaqueGreatest quantity when plaque is being transformed into calculus

Calcium and phosphorus are main

Small amounts of Magnesium, potassium and sodium

Fluoride when there is topical application

Formation and biochemistry:

First layer that is formed on tooth is called PELLICLEThis is the organic structure formed prior to bacterial colonization

Significant difference in pellicle formed on natural teeth and that on artificial surfaces

Therefore composition may vary as per the host site

Stage I adsorption of salivary proteins to apatite surfaces

By electrostatic ion interaction of calcium ions and phosphate groups in the enamel

surface and oppositely charged groups in the salivary molecules.Composed of glycoproteins

Immunoglobulins

Different carbohydrates


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Stage II transition from dental pellicle to dental plaque

Colonization of pellicle by bacteriaFirst colonizers cocci

Epithelial cells (few)

Polymorphonuclear leukocytes

Forms a monolayer of cells, either singly or in groups

Bacterial growth spreads laterallyCoalescing with neighboring patchesGiving rise to different micro colonies in a complex pattern

Bacterial adherence:

First bacteria must adhere too the pellicle surface

Become sufficiently attached to withstand the oral cleansing forces

Second they must grow and adhere to each other

Electrostatic forces: negatively charged components of the bacterial cell surface

and negatively charged surface glycoproteins in pellicle become linked via

calcium cations

Hydrophobic interactions: based on close structural fit between molecules

Organic solutes: salivary glycoproteins have specific receptors called adhesions

which promote chemical bonding between some bacteria and pellicle and inhibitother bacteria.

Bacterial Growth and Proliferation: leads to bacterial accumulation

leads to increase in plaque mass

characterized by multiplication and cohesion of bacterial cells

increase in bacterial byproducts and thus changes in intercellular matrix

depends uponbacterial factors:

-bacteria like S. mutans produce extracellular glucans which are sticky and causeentrapment of other bacteria.

- Some bacteria produce compounds that are essential nutrients and growth

factors for other microorganisms.

- Some species produce bacteriocin which is inhibitory for adhesion of othertypes

- The prevailing bacteria will utilize all available nutrients and not leave any for

survival of other similar species

Environmental factors:

Low pH: fermentation of carbohydrate causes low pH, thus only those bacteria

able to survive in this environment will predominate. (caries)O2 tension: streptococcus and lactobacillus consume the available oxygen. As

their umber increases the oxygen tension decreases resulting in a shift towards

obligatory anaerobes. Similarly changes in temperature can take place facilitatin

or inhibiting future bacterial growth.

Salivary nutrients which are present in the pellicle and the surrounding saliva

will determine the changes in bacterial pattern.Host factors:

Oral cleansing mechanism, like salivary flow, mastication and movement of

tongue and cheek.


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Saliva contains bacterial inhibitory substances like lactoperoxidase, lactoferrin,

and lysozyme which prevent accumulation of sensitive bacteria.

Host response factors like antibodies, leukocytes and complement in the GCF dnot allow bacterial adhesion and proliferation.

Clinical Significance: if the supragingival plaque is not allowed to mature, then one can expect health

in gingival tissues

in case the plaque is allowed to mature, it results in gingivitis and the subsequent formation o

subgingival plaque.

So in early periodontitis, the supragingival plaque strongly influences the growth,

accumulation and pathologic potential of subgingival plaque

Once the pocket has formed and disease has progressed, the influence of supragingival plaqu

on activity of subgingival plaque is limited to the most coronally situated part only

SUB-GINGIVAL PLAQUE:

Definition: that dental plaque which is present in the gingival sulcus or periodontal pocket

Structural Characteristics:Stagnant environment, less subject to natural cleansing activities of the mouth

Thus even those micro organisms which do not readily attach to hard surfaces are allowed to

colonize and proliferate.

These can adhere to the tooth surface or to pocket epithelium.

More nutrient supply: those in relation to pocket epithelium have more direct access to nutrients

especially the proteins of sulcular fluid

Lower oxidation-reduction potential: environment has lower oxidation-reduction potential, thus

allowing anaerobic bacteria to establish more easily


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Bacterial invasion of connective tissue: bacteria from epithelium associated plaque may penetrat

and colonize the gingival connective tissue, and may also inhabit the alveolar crest as the

periodontitis

Types:

1. Tooth Associated(attached) Sub-Gingival Plaque

2. Epithelium Associated Sub-Gingival Plaque

3. Unattached Sub-Gingival Plaque

Tooth Attached Sub-Gingival Plaque:

Gram +ve bacteria predominate, densely packed and at right angles to the root surface,

structure similar to supra-gingival plaque with granular like surface

Rods and cocci like Streptococcus mitis, S sanguis, Eubacterium, Bifido-bacterium,

Actinomyces viscosus, A naeslundi, Propionibacterium.

Few gram negative cocci and rods, especially in the more apical portions.Does not extend to junctional epithelium, between the junctional epithelium and apical

border of plaque there is accumulation of leukocytes.

May penetrate cementum

Associated with mineral deposition and calculus formation besides root caries and root

resorption

Epithelium Associated Sub-Gingival Plaque:

Gram variable, gram negative rods and cocci, flagellated bacteria and spirochetes, no

specific pattern.Bacteriodes, Fusobacterium, Capnocytophaga, Selenomonas, Campylobacter,

Actinobacillus

Loosely adherent in direct association with epithelial wall of pocket from gingival margin

extending upto junctional epithelium

May penetrate epithelium and connective tissue

Associated with gingivitis and periodontitis

Unattached Sub-Gingival Plaque:


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Gram variable

Extends upto junctional epithelium

Associated with gingivitis

Characteristics of Sub-Gingival plaque

Attached to Tooth Unattached Attached to Epithelium

Gram positive bacteria

predominate

Gram Variable Gram variable

Bacteria organized perpendicular

to tooth surface

Not organized Not organized

Does not extend upto junctional

epithelium

Extends upto junctional

epithelium

Extends upto junctional

epithelium

May penetrate cementum - May penetrate epithelium and

connective tissue

Associated with calculus

formation and root caries

Associated with gingivitis Associated with gingivitis and

periodontitis

Bacterial Invasion of Periodontium:There is evidence of bacterial invasion into gingival in gingivitis and ANUG

Through lateral wall of periodontal pockets

Through the junctional epithelium in advanced periodontitis and LJP

Penetration through ruptured intercellular spaces of stratum spinosum. Basal lamina is sort

the barrier for such penetration. Such penetration through basal lamina is through

perforations or interruptions in it or through ulcerations in pocket wall or through

microholes through which leukocytes migrate across

Gram negative and positive cocci, rods, filaments and spirochetes have been found in

connective tissue and also in contact with crest of alveolar bone in advanced disease.

Advancing Front: plaque adjacent to the sulcular and junctional epithelia is the advancing

front of periodontitis disease. Active lesions in rapidly progressive diseases contain gram

negative motile organisms

bursts of activity might be the result of periods of active bacterial penetration and

subsequent tissue destruction.

Calculus has only an indirect role in periodontal disease. It has on its surface the plaque an

allows it to be more in contact wit pocket walls. Causes irritation and physical trauma to

thin inflamed pocket epithelium. Allows easier entry of plaque bacteria

Pocket wall is constantly changing as per the disease activity. There are microscopic areas

of (1)heavy bacterial accumulation, (2)host response, (3)emergence of leukocytes,

(4)leukocyte-bacterial interaction, (5)evidence of tissue destruction like hemorrhage &

ulceration (6)epithelial desquamationClinical implication: in localized juvenile periodontitis mechanical periodontal therapy do

not eliminate Actinobacillus actinomycetemcomitans from the tissues, and therefore

systemic antibiotics along with surgical therapy is needed to eliminate the bacteria

Concept of Microbial Specificity:

Before composition of plaque was thought to be similar from patient to patient and from sit

to site.


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But in some cases a lot of plaque caused little destruction as in case of chronic periodontitis

while in cases like localized juvenile periodontitis and pre-pubertal periodontitis little

detectable plaque was present with dramatic loss of periodontium.Loesche 1976 Specific plaque hypothesis

Specific forms of periodontal diseases have specific bacterial causesThe concept of bacterial specificity suggests that periodontal disease may be a group of diseases

with different causes and clinical courses but with similar symptoms

Technical difficulties in studying Sub-Gingival flora:

1. Sampling: curette or scalar

Paper point

2. Dispersion: adherent micro organisms have to separated from each other without losing

their viability

3. Cultivation: need different selective and non selective media for growth of different

micro flora, especially the facultative and obligatory anaerobes andmicroaerophillic

4. Identification of Microorganisms: need identification and characterization of different

bacteria

5. Statistical Analysis: complex and voluminous data need accurate analysis

Mechanism of Bacterial Mediated Destruction:

Health= Host-parasite equilibrium in favor of host

For disease to happen

Need bacterial colonization & proliferation

Need bacteria to maintain themselves

Need bacterial penetration and invasion into connective tissue

Need toxicity effects of bacteria to occur through toxins, enzymes, or metabolic produc


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Need to spread the organisms orproducts in the connective tissue

Need bacteria to suppress/evade host immunity by inhibiting PMN chemotaxis

Phagocytosis/bactericidal activit

interbacterial activity may give rise to favorable or inhibitory bacterial succession

Direct Toxicity:

Toxins:Exotoxins: Released by bacteria in surrounding environment

Protein type

Cause direct tissue injury

Epitheliotoxins

Leukotoxins

Endotoxins: structural components of Gm ve bacteria release after bacterial lys

Lipo-polysaccharidesAmplify inflammatory process

Can produce localized leucopenia

Can activate Factor XII, causing intra vascular coagulation

Can activate complement system by alternative pathway

Can cause localized Shwartzman phenomenon and necrosis

Cytotoxic to fibroblastsMaybe induce bone resorption

Cell Constituents: bacterial surface components & capsular components

peptidoglycan

Activates host tissue response like complement

Immunosuppression

Stimulates Reticulo Endothelial SystemIndirectly stimulates collagenase production from macrophages

Causes tissue destruction and bone resorptionAllows bacteria to evade host protective system

Enzymes: facilitate tissue penetration by bacteria

Proteases: collagenase, hyaluronidase, chondroitin sulfataseOthers like Alkaline & acid phosphatase, phospholipase, aminopeptidases

End products of bacterial metabolism: contribute to inflammatory process

Volatile sulfur compounds, ammonia, indole, fatty acids, polyamines

Indirect Toxicity:

Local immune reaction triggered by bacteria or their products cause tissue destruction

Bacterial Factors In Evasion of Host Defenses:

Inhibition of PMN: Leukotoxin

Chemotaxis inhibitors

Decreased Phagocytosis and intracellular killing

Resistance to C-mediated killingLymphocyte alterations

Endotoxicity

IgA, IgG proteases


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Fibrinolysin

Superoxide dismutase

Catalase

Microbiological Flora in Health and Disease:

Oral Flora in normal mouths:Microorganisms from water, food, air, etc gain ready accessIdeal temperature and pH and oxygen tension

Abundant supply of nutrients

Oral cavity is sterile at birth

Simple facultative flora within 6-10 hours

Anaerobes within first 10 days to 5months and definitely when incisors appearBesides bacteria there are Fungi like Candida, Cryptococcus, Saccharomyces

Protozoa like Entamoeba gingivalis, Trichonomas tenax

Viruses

Mycoplasma

Only bacteria that are able to attach and resist detachment are retained and colonize.Bacteria preferentially colonize specific anatomic locations based on their adherence

characteristics, complex growth requirements. As the micro-environmental conditions change

in favor of another species, the original species must either adapt to new conditions of be

superseded by the next species which is better suited to colonize and proliferate in the newer

conditions bacterial succession

Periodontal health = Gm +ve cocci and rods

Supragingival plaque initiated by Streptococcus sanguis & other Gm +ve cocciActinomyces viscosus another one of important initial colonizer

Secondary growth and proliferation

Bacterial succession or bacterial population shift occurs

(Streptococcus mitis, Staphylococcus epidermidis, Rothia dentocariosa, A naeslundi and fewspecies of Neisseria & Veilonella)

Very few Gm ve organisms like Capnocytophaga, Prevotella loeschii, Campylobacter,

Fusobacterium and spirochetes like Treponema denticola

In healthy periodontium the non pathologic organisms predominate and dont allow the

periodontopathogens to colonize, protective species(S sanguis, S uberis, Veilonella parvula, R dentocariosa, Capnocytophaga ochracea,

Propionobacterium acnes)

Gingivitis:

Increase in supragingival plaque

Change from gram +ve (mainly cocci) to a more complex flora including substantial Gm veand spiral motile forms in a sequential form of succession.

Gm +ve bacteria like Streptococcus sanguis, S mitis, S intermedius, S oralis, Actinomyces

viscosus, A naeslundi, Peptococcus micros.


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Gm ve bacteria like Fusobacterium nucleatum, Prevotella intermedia, Veilonella parvula, &

few Hemophillus, Capnocytophaga, Campylobacter species and few Treponema denticola

Initially edematous changes in marginal gingivalAdvanced stages may have bacterial penetration in gingival epithelium and connective tissue.

Pregnancy Gingivitis:

Prevotella intermedia

Porphyromonas gingivalisCapnocytophagaIncrease in hormones like estrogen and progesterone which act like nutrient source for these

bacteria

ANUG:

pathophysiology of disease as being caused by a fusospirochetal complex that requires

underlying tissue changes to facilitate the pathogenic activity of the bacteria.Treponema microdentium,

Borrelia vincenti, intermediate size spirochetes, vibrios, fusiform bacilli,

Prevotella intermedia

Actinomyces odontolyticus

Selenomas species

Chronic Periodontitis:

Increase in loss of attachment

High percentage of anaerobic (90%) species

Gm ve are more preponderant in plaque = 75%

Porphyromonas gingivalis, (elevated in active sites, associated with disease progression

Prevotella intermedia, (elevated in active sites, associated with disease progression)Bacteroides forsythus, (elevated in active sites, associated with disease progression)

Campylobacter rectus, (elevated in active sites, associated with disease progression)Actinobacillus actinomycetemcomitans, (associated with disease progression)

Eikenella corrodens,

Fusobacterium nucleatum, (elevated in active sites)

Peptococcus micros,Treponema denticola and other species

Eubacterium species

Bacteria noted in connective tissue: P gingivalis, A actinomycetemcomitans.

Rapidly Progressive Periodontitis:

Young adults 20-35years of ageGeneralized, severe and rapid bone loss

Small amounts of plaque

Porphyromonas gingivalis, Prevotella intermedia, Bacteroides capillus

Actinobacillus actinomycetemcomitans, Eikenella corrodens, Wolinella recta

Localized Aggressive Periodontitis:

Rapid and severe loss of attachment in individuals during or after puberty

Complicated by some diminished host response functionPrePubertal Periodontitis:


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Rare form

Immediately after eruption of primary teeth

Patients have severe defects in neutrophils and macrophagesActinobacillus actinomycetemcomitans is predominant

Capnocytophaga sputigena, Prevotella intermedia, Eikenella corrodensLocalized Juvenile Periodontitis:

Adolescents

Rapid destruction of periodontium around incisors and molars (arc shaped)90% bacteria in Localized Juvenile Periodontitis is A actinomycetemcomitansOther: P gingivalis, E corrodens, C rectus, F nucleatum, Bacteroides capillus,

Eubacterium brachy, Capnocytophaga species, and spirochetes

A actinomycetemcomitans produces a neutrophil inhibiting toxin = leukotoxin

Refractory periodontitis:

Does not respond to conventional treatmentPorphyromonas gingivalis

A. actinomycetemcomitans, Peptococcus micros, Wolinella recta, Bacteroides forsythus,

Prevotella intermedia, Eikenella corrodens

Periodontal Abscess

Acute lesionWith or without concomitant periodontitis

Fusobacterium nucleatum, Prevotella intermedia, Porphyromonas gingivalis,

Peptococcus micros, Bacteroides forsythus

Immunology of Periodontal Disease:

Bacteria and Host Defense interactionMay be beneficial by protecting against the spread and effects of bacteria

May be detrimental by contributing to tissue damage

Host defense variables try to influence bacteria at every step

- bacterial colonization

- bacterial invasion- tissue destruction

- healing and repairBacterial colonization:

IgG and complement present in GCF to fight against subgingival plaque bacteria

Inhibits adherence and co-aggregation

Maybe reduce number by lysisExplosion of bacteria increases antigen load

immune system may get overwhelmedBacterial Invasion:

Only few bacteria traverse across epithelium into connective tissue

Tissue are having plenty of antibodies and complement

Chemotaxis of PMN and monocyte infiltrationLeading to phagocytosis and lysis of bacteria

Patients having defects of neutrophil and macrophage function and chemotaxis have diseaseTissue Destruction:


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Antibody mediated hypersensitivity type release of histamine

Cytotoxic reactions by IgG and IgM and complement

Immune microcomplex reactions by IgG & IgM activates complement leading to hormonal,vascular and cytotoxic events and lysozyme release

Cell mediated reactions by sensitized T lymphocytes resulting in release of lymphokines,

interleukins (IL-1) and osteoclast activating factor,

Activation of tissue factors like collagenase

Healing and fibroblasts:Lymphocyte and macrophage produced chemotactic factors for fibroblastsRelease of lymphokines like fibroblast activating factors

Some Bacteriodes produce proteases which inactivate antibodies, or stimulate OAF production

or activate T suppressor cells

Immunologic Changes in health and periodontal disease:

Health: presence of chronic inflammatory cells and low titres of antibodies

Chronic disease: increase in Gm ve, filamentous and spirochetes

Increase in B cells, Mast cells, Complement, Inflammatory cells, Prostaglandins,

Enzymatic action, and tissue destruction

Increase antibodies to P gingivalis and other periodontopathogens

Increase in immune complexes in tissuesImmediate hypersensitivity to gingival bacteria

Cell mediated immunity to gingival bacteria

ANUG: PMN chemotactic defect

Increase antibodies to Prevotella intermedia and intermediate spirochetes

Localized Juvenile Periodontitis: PMN chemotactic defect

Decrease in ability for PhagocytosisPMN cellular abnormality

Increase immunoglobulins to A actinomycetemcomitans serotype B and little serotypeA

Increase in leukotoxin production by the bacteria

Generalized Juvenile Periodontitis: PMN chemotactic defect

Decreased phagocytosis but normal migration

Increase IgG to Porphyromonas gingivalis, with increase in protease activity

Increase antibodies to A actinomycetemcomitans serotype C

PrePubertal Periodontitis: increased WBC countDecreased PMN and monocyte chemotaxis

Decreased adherence

Increased functional defects

Periodontitis in Juvenile Diabetes:Neutrophil chemotactic defect.

Rapidly Progressive Periodontitis: suppressed or enhanced PMN or monocyte chemotaxis

Increased antibody levels to several Gm ve bacteria


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Refractory periodontitis: decreased PMN chemotaxis

Periodontal Abscess: same as adult periodontitis

Desquamative Gingivitis: diagnostic or characteristicimmunopathologic changes

Autoimmune etiopathogenesis in pemphigus and pemphigoid cases

AIDS and ANUP: altered T4: T8 ratio

Neutrophil Related Periodontal Disease:

Periodontal Disease with Neutrophil Disorder:

1. ANUG

2. Localized Juvenile Periodontitis

3. PrePubertal Periodontitis4. Rapidly Progressive Periodontitis

5. Refractory Periodontitis

Neutrophil disorders associated with Periodontal Disease

Primary:

1. Cyclic Neutropenia2. Chediak Higashi syndrome

3. Leukocyte Adhesion Deficiency (LAD-1)

4. Agranulocytosis or Chronic Granulamatous Disease (CGD)

Secondary:

1. Diabetes Mellitus

2. Papillon Lefevre Syndrome3. Down syndrome

4. AIDS5. Pre Leukemic syndrome

6. Acute Myeloid Leukemia

7. HyperImmunoglobenemia E (Jobs syndrome)

Future Advances in Study of Periodontal Microbiology:

Plaque Assays:

ii) phase and darkfield microscopy

iii) culture and isolation

iv) identification of bacterial enzymes and products

v) immunofluorescencevi) latex agglutination

vii) ELISA

viii) immunoblotting

ix) DNA probes :DNA based methodology to identify and detect specific bacteria and

viruses

- no need for cultivation- more samples can be examined

- more amount of data

- detect even those organisms that are sensitive to dispersion, sampling, culture.


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Indirect Assays on Sera:

i) Immunofluorescence

ii) ELISA

Corn-cob formation: rods like Bacterionema matruchotii & Fusobacterium nucleatum

Cocci like streptococci and Porphyromonas gingivalis

Interbacterial interaction

Fimbriae

Coaggregation

Van der Wahls forces


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Summary of Events

1

Initial colonization by pioneer species

2

Outgrowth, microcolonies are formed which spread outwards and upwards

Secondary colonisation and multiplication. Species diversity increases. Theproportion of streptococci decreases as the plaque is invaded by bacteria from

other genera. The overall cell density decreases and the space between cells isoccupied by polymers.

Climax Community

This transmission electron micrograph of a section through mature dental plaque illustrates

some important features . Note the densely packed palisades of cells at the base of theplaque. These are almost always seen to have thick cell walls characteristic of cells which

are slow growing due to starvation conditions. Above these the plaque is less denselypacked with cells and there is an increase in species diversity illustrated by the presence of

rod-shaped organisms. Electron-dense material between cells are high molecular weight

polymers such as extracellular polysaccharides synthesised from sucrose. Within the body ofplaque microcolonies are often featured. The one labelled above is more visible than others


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because it has a very different morphology.


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